ArticleInternational journal of molecular medicine2016
Jumonji AT-rich interactive domain 1B overexpression is associated with the development and progression of glioma.
Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Retraction Note: m6A demethylase ALKBH5 inhibits pancreatic cancer tumorigenesis by decreasing WIF-1 RNA methylation and mediating Wnt signaling.Molecular cancer · 2025Article
- Article
- KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic.Advances in experimental medicine and biology · 2023Article
- Review
- Article
- KDM5A and KDM5B histone-demethylases contribute to HU-induced replication stress response and tolerance.Biology open · 2021Article
- SNHG1 promotes malignant biological behaviors of glioma cells via microRNA-154-5p/miR-376b-3p- FOXP2- KDM5B participating positive feedback loop.Journal of experimental & clinical cancer research : CR · 2019Article
- Prognostic significance of RBP2-H1 variant of JARID1B in melanoma.BMC cancer · 2017Article
Corrections and comments
- Correction · 2016-07-15Error in Data · Error in Image · Updated to Retraction · · see also: https://pubpeer.com/publications/CEDE2BB6FF7415B557E447E93C6658
- Retraction · 2024-09-16Author Unresponsive · Concerns/Issues about Image · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Plagiarism of Image · Upgrade/Update of Prior Notice(s) · · see also: https://pubpeer.com/publications/CEDE2BB6FF7415B557E447E93C6658
- Erratum issued
- Retracted
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have suggested that jumonji AT-rich interactive domain 1B (JARID1B) plays an important role in the genesis of some types of cancer, and it is therefore considered to be an important drug target protein. Although the expression of JARID1B has been researched in some types of cancer, little is known about JARID1B expression in glioma and its function in the tumorigenesis of gliomas. In the present study, we examined the expression of JARID1B in glioma. In addition, RT-PCR, western blot analysis and immunohistochemical analysis were performed using glioma tissue samples and the results revealed that JARID1B expression increased according to the histological grade of glioma. However, in the normal brain tissue samples JARID1B expression was barely detected. Kaplan‑Meier analysis revealed that higher JARID1B expression in patients with glioma was associated with a poorer prognosis. The overexpression of JARID1B stimulated the proliferation and migration of glioma cells as well as sphere formation, whereas suppressing the expression of JARID1B produced opposite effects. The overexpression of JARID1B increased the tumorigenicity of glioma cells in vivo in a nude mouse xenograft model of glioma. Moreover, the activation of phosphorylated (p-)Smad2 contributes to JARID1B-induced oncogenic activities. These findings suggest that JARID1B is involved in the pathogenesis of glioma, and that the downregulation of JARID1B in glioma cells may be a therapeutic target for the treatment of patients with glioma.
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Registered trials
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